Heterotropic Ossification

44
Heterotropic Ossification Dr K.Raghuveer Adiga

description

Heterotropic Ossification. Dr K.Raghuveer Adiga. Hetrotropic ossification was first described in 1692 by Patin in children with myositis ossificans progressiva Clearer description was provided by Reidel in 1883 Dejerine and Ceillier in 1918. - PowerPoint PPT Presentation

Transcript of Heterotropic Ossification

Page 1: Heterotropic  Ossification

Heterotropic Ossification

Dr K.Raghuveer Adiga

Page 2: Heterotropic  Ossification

• Hetrotropic ossification was first described in 1692 by Patin in children with myositis ossificans progressiva

• Clearer description was provided by Reidel in 1883 Dejerine and Ceillier in 1918

Page 3: Heterotropic  Ossification

During Ist World war, HO was predominantlyobserved in soldiers who had become paraplegicdue to gunshot wounds.

Page 4: Heterotropic  Ossification

Based on hypothetical etiopathogentic mechanism several terms used to denote this condition

Ectopic ossification Myositis ossification Neurogenic ossifying fibromyopathy Paraosteoarthropathy Periarticular ossification

Page 5: Heterotropic  Ossification

• Myositis ossificans refers to a condition in which ectopic bone is formed within muscle and other soft tissues

• Robert(1968)reported HO in a patient with cerebral injury. Elbow was the involved joint.

Page 6: Heterotropic  Ossification

Clinically: Fever, swelling, erythema Decreased joint movt seen in early HO which may mimic; Cellulitis Osteomyelitis Thrombophlebitis Osteosarcoma Osteochondroma

Page 7: Heterotropic  Ossification

ClassificationTwo versions: - Acquired

- Hereditary

Acquired form: A) Trauma:1) Fracture

2)THA

3)Direct muscular injury

Page 8: Heterotropic  Ossification

B)Neurogenic:1) Spinal cord injury

2) Head injury

Hereditary: Myositis ossificans progressiva

Page 9: Heterotropic  Ossification

Heterotopic ossification of the hip is graded

according to Brooker’s Grading scale

• Grade 1. Islands of bone within the soft tissues about the hip.

• Grade 2. Bone spurs in the pelvis or the proximal end of the femur with at least 1 cm between the opposing bone surfaces.

• Grade 3. Bone spurs from the pelvis or proximal end of the femur with <1 cm between the opposing bone surface.

• Grade 4. Radiographic ankylosis.

Page 10: Heterotropic  Ossification

Rare causes: Following burns Sickle cell anemia Hemophilia Tetanus Poliomyelitis Multiple sclerosis Toxic epidermal necrolysis

Page 11: Heterotropic  Ossification

Incidences: Following THA 16% to 53% SCI 20% to 30% Closed head injury 10% to 20% Spastic limb 11% to 76% Usually HO forms after THA is minor andclinically not significant

Page 12: Heterotropic  Ossification

• Garland found that 89% joints involved were in spastic limbs

• Hip joint being most common

Page 13: Heterotropic  Ossification

HO @ other sites:

THA 16 to 53%TKA 9%Elbow 10 to 20%

Page 14: Heterotropic  Ossification

Aetiology• Extact cause is unknown

• Pleuripotential mesenchymal cells → Osteoblasts

• This causes HO

• Bone morphogenetic protien → differenitation of mesenchymal cells → bone

Page 15: Heterotropic  Ossification

• Occur within 16 hours of surgery, peaks at 32 hours.

• Reaming → bone marrow + traumatised well vascularized muscle → HO.

Page 16: Heterotropic  Ossification
Page 17: Heterotropic  Ossification

Head injury patient needs ventilation↓

Ventilation known to cause homeostatic changes of systemic alkalosis

↓This modifies precipitation kinetics of calcium

and PO4 ↓

Page 18: Heterotropic  Ossification

Modifying pH at fracture sites ↓

Acidity to alkalinity ↓

More callus ↓

H O

Page 19: Heterotropic  Ossification
Page 20: Heterotropic  Ossification

Urist in 1978 discovered that dimineralisedbone matrix could invoke bone formation ectopically and postulated a small (0.025mm)hydrophobic bone morphogenic protein the causative agent capable of changing mesenchymal cells in muscle from fibrous tissueto bone.

Page 21: Heterotropic  Ossification

Chalmers (1975) described three condition necessary for HO formation 1) Osteogenic precursor cells 2) Inducing agents 3) Premissive enviornment

Page 22: Heterotropic  Ossification

Contributory factors

• Hypercalcemia• Tissue hypoxia• Change in sympathetic nerve activity• Prolonged immobilization• Mobilization after prolonged immobilization• Disequilibrium between PTH and calcitonin

Page 23: Heterotropic  Ossification

Biochemical changes:

Alk PO4 levels - ↑ 3 ½ times at 4 weeks post injury

PGE2 excretion in 24 hour urine-early indicator of HO

Page 24: Heterotropic  Ossification

Histology:

Myositis ossificans and HO are fundamentally different.

Important steps in the ossification process is fibroblastic metaplasia.

Page 25: Heterotropic  Ossification

Histological studies clearly demonstrates a zone of fibroblastic proliferation, followed by chondroblasts which eventually transformed into osteoblasts with blood vessels and haversian canals.

Page 26: Heterotropic  Ossification

Diagnosis and Investigations• Alk PO4 ase levels

• Three phase bone scintigraphy

- Diagnostic and therapeutic follow up

-very sensitive.

- Usually positive after 2-4 weeks.

- Serial bone scan helps to monitor of metabolic activity.

Page 27: Heterotropic  Ossification

• Radiography, MRI and CT scan

• Ultrasonography - < one week after THA

Page 28: Heterotropic  Ossification

Treatment

1) Physiotherapy:

-Assisted range of movement exercise with gentle stretch and terminal resistance training.

-Joint movement not beyond pain free range

Page 29: Heterotropic  Ossification

2) Medical management:

NSAIDs Indomethacin 25mg tds for 6 weeks

COX2 inhibitors:Meloxicam 7.5mg/15mg per day

Page 30: Heterotropic  Ossification

Bisphosphonates

retards the ossification

when drug is stopped, osteoid gets mineralized

Etidronate-300mg/day/IV for 3 days, then 20mg/kg/day for 6 months

.

Page 31: Heterotropic  Ossification

3) Radiation Therapy

Extact mechanism is not known.

Supposed to interfere with the differentiation of pleuripotent mesenchymal cells into osteoblasts.

Page 32: Heterotropic  Ossification

Coventry and Scanlon(1970)-offered preventive radiation therapy for the first time at Mayo clinic before performing THA.

Page 33: Heterotropic  Ossification

20 Gy in 10 fractions was the dose used initiallybecause >20 Gy inhibited vertebral growth in children.

Now 7 Gy in single fraction radiation found to very effective..

Page 34: Heterotropic  Ossification

Timing

Within 72hours after surgery. After 72 hours mesenchymal cells become differentiated.

Pre -op Radiation vs Post operation Radiation7 Gy 4 hrs before surgery vs 7Gy < 72 hours after surgery showed no difference in outcome.

Page 35: Heterotropic  Ossification

Shielding the prosthetic device is very importantduring radiation therapy

Page 36: Heterotropic  Ossification

Side effect of Radiation

If the doses are 30 Gy and above,

Radiogenic tumors induction

Fertility problems

Page 37: Heterotropic  Ossification

4) Surgical Treatment

Only after HO has reached maturity

HO become less metabolically active and

has decreased rate of bone formation.

Page 38: Heterotropic  Ossification

Garland(1991) has recommended schedules for surgical intervention.

6 months- after direct traumatic musculoskeletal injury

1 year-after spinal cord injury

1 ½ years-after traumatic brain injury

Page 39: Heterotropic  Ossification
Page 40: Heterotropic  Ossification
Page 41: Heterotropic  Ossification

6 months period is essential for bone to mature + distinct fibrous capsule to develop

↓This minimizes trauma to surrounding structure

↓Prevent hematoma formation

↓Decreases local recurrences of HO

Page 42: Heterotropic  Ossification

Complete wound lavage↓

Avoid soft tissue trauma↓

Remove all bone debris↓

Reaming is also thought to decrease HO

Page 43: Heterotropic  Ossification

Ghent university Protocol:

Prior to THA or resection of HO, single dose radiation therapy given.

NSAIDs given after surgery.

Rationale of irradiation is to reduce pre-op and post-op bleeding.Post op irradiation not given.

Page 44: Heterotropic  Ossification

Finally, HO • Poorly understood condition• Little known exact mechanism • Development can be reduced by physio,

NSAIDs and occasional radiotherapy.• Excision may give good results. But there is

risk of recurrence.